AV shunt (less common)

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Transcript AV shunt (less common)

ACUTE RENAL FAILURE
CHRONIC RENAL FAILURE
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What does the kidney do in terms of?
 wastes and water balance?
 Acid base balance?
 Controlling BP?
 Controlling anemia?
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 Kidneys
no longer function properly
 Kidneys unable to excrete waste
 kidneys cannot concentrate urine
 Kidneys cannot conserve electrolytes
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GLOMERULAR FILTRATION:glucose, amino acids,
creatinine, urea, phosphates, uric acid
GLOMERULAR REABSORPTION:bicarbonate,
phosphates, sulfates, 65% of Na and water, glucose, K,
amino acids, H ions, urea
GLORMERULAR SECRETION: hydrogen and
potassium, remove acids (hydrogen) to maintain
appropriate acid base balance, potassium, urea
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u/a: negative for glucose, protein, blood,
leukocytes, nitrites, ketones
Specific gravity: measures concentration of
the urine; normal values: 1.010-1.025
Urine osmolality: normal 300-900 mOsm/
kg/24
Serum creatinine: 0.6-1.2mg/dl
BUN: 7-18mg/dl
BUN to creatinine ratio: about 10:1
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 OLIGURIA:
 POLYURIA:
 ANURIA:
 NORMAL
URINARY OUTPUT:
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 PRERENAL
or factors external to the kidney
which interferes with renal perfusion (55%
cases of ARF)
 INTRARENAL: conditions
that cause direct
damage to renal tissue (35-40% cases of ARF)
 POSTRENAL: mechanical
obstruction in the
urinary tract (5% cases of ARF)
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 Multiple
problems may exist at same
time
 AGING
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 Retention
of metabolic wastes
 Imbalance of fluid and electrolytes
 Alterations of sensorium
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 Oliguria
 Diuresis
 Recovery
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Urinary changes
Fluid volume excess
Metabolic acidosis
Sodium balance
Potassium excretion
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 Hematologic
disorders
 Calcium deficit and phosphate excess
 Waste product accumulation
 Neurologic disorders
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Gradual increase of urine output as a result
of osmotic diuresis
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 Do
all patients recover?
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 Restore
renal function
 Identify cause
 Eliminate cause
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 How
do we assess fluid excess?
 How can we control fluid intake?
 What physical assessments would be
done?
 What would you expect to see?
 What laboratory tests would be used to
assess client status?
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Elevated serum phosphate:
Hypocalcemia:
Hypermagnesemia:
Hypovolemia:
Fluid retention: diuretics:
Hypertension:
Metabolic acidosis:
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 Regular
insulin IV
 Sodium bicarbonate
 Calcium gluconate IV
 Dialysis
 Kayexalate
 Dietary restriction
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 dietary
protein
 calories
 K and phosphorus
 Na
 Fe
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 Progressive
deterioration in renal
function resulting in fatal uremia (excess
of urea and other nitrogenous wastes in
the blood)
 Irreversible destruction of nephrons
 Called ESRD (end stage renal disease)
 Dialysis or transplant
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 Azotemia: collection
of nitrogenous
wastes in blood
 Uremia: azotemia
 Uremic syndrome: systemic clinical and
laboratory manifestations of ESRD
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Metabolic Disturbances:
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elevated BUN,
creatinine,
hyponatremia,
hyperkalemia,
metabolic acidosis,
hypocalcemia,
hyperphosphatemia
Integumentary Disturbances: pruritus,dry,hair brittle,
nails thin, UREMIC FROST: white/yellow crystals of
urate on skin
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 Gastrointestinal
Disturbances: Anorexia, N&V,
metallic taste in mouth, breath smells like
ammonia, stomatitis, ulcers/GI bleeding,
constipation
 Neurological Distrubances: uremic
encephalopathy progresses to seizures & coma
 CHF: from increased workload on heart from
anemia, hypertension and fluid overload
 Uremic pericarditis: pericardium becomes
inflammed from toxins
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 Respiratory:
• breath smells like urine: uremic fetor or uremic
halitosis
• Metabolic acidosis: see tachypnea (increased
rate) and hyperpnea (increased depth) indicates
worsening metabolic acidosis
 See Kussmaul respirations extreme hyperventilation
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FOR ANEMIA:
FOR HYPOCALCEMIA
FOR FLUID RETENTION AND HYPERTENSION
FOR SKIN ITCHING
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 calorie
 protein
 Na
K
 calcium
 Phosphorus
 Magnesium
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Diffusion of solute molecules through a semipermeable membrane passing from the side of higher
concentration to that of lower concentration
Fluids passing through the semi-permeable membrane
via osmosis
Renal Failure pt has dialysis to remove waste products
and to maintain life until kidney function can be
restored
Dialysis indicated for high levels of K and fluid
overload
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 Sterile
dialyzing fluid is introduced into
the peritoneal cavity
 Peritoneum is an inert semipermeable
membrane
 The dialyzing solution promotes osmosis
leading to diuresis
 Urea and creatinine are removed
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Baseline VS and wgt
Assess for fluid overload
Maintain highly accurate inflow and outflow
records
When PD starts the outflow may be bloody or
blood tinged
This clears within a week/two
Effluent should be clear and light yellow
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Drainage bag is lower than the client’s
abdomen to enhance gravity drainage
Avoid kinking or twisting, ensure clamps
are open
Reposition client to stimulate inflow or
outflow
Sitting/standing/coughing: increases
intraabdominal pressure
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Respiratory difficulties
Hypotension
Infection:
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peritonitis: see cloudy or opaque dialysate outflow (effluent),
fever, abdominal tenderness, pain, malaise, N&V
Hypo-albuminemia
Bowel perforation:
Bladder perforation:
Catheter may get clogged
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 Fibrin
Clot formation
 Milking the tubing
 Xray
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 Dialysate
leakage
 See with obese, diabetic, older clients,
those on long term steroids
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 Process
by which the uremic toxins and
accumulated waste products are
removed from the blood
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A
synthetic semi-permeable membrane
replaces the renal glomeruli and tubules
and acts as a filter for the impaired
kidneys
 Must have 3 times/week for 4 hours per
treatment for rest of life
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 AV
shunt (less common): external silastic
tubing placed in an adjacent artery and vein
 AV Fistula: internal access using pts own
vessels (artery and vein)
 AV Graft: internal access using a foreign
material
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 BLEEDING
 INFECTION
 CLOTTING
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Assess for disequilibrium reaction
CAUSE:
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due to rapid decrease in fluid volume and BUN levels
Change in urea levels can cause cerebral edema and
increased intracranial pressure
Neurologic complications: HA, N&V, restlessness,
decreased LOC, seizures, coma, death
PREVENTION: starting HD for short periods
with low blood flows
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 Vasoactive
drugs which cause
hypotension are held until after treatment
 CHECK WITH PHYSICIANABOUT WHICH
DRUGS TO BE HELD
 Know pt’s BP pre-dialysis
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BP and wgt
Hypotension
Temperature may also be elevated:
If client has a fever
Bleeding risk:
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 Involves
transplanting a kidney from a
living donor or human cadaver to a
recipient who has end-stage renal
disease and requires dialysis to live
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major concern is rejection
 Drugs given to suppress immunologic
reactions: Imuran, prednisone,
cyclosporin (Cyclosporin A)
Next concern is infection
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TO DETECT REJECTION:
 Assess for increased temp, pain or
tenderness over grafted kidney
 Assess for decrease in urine output,
edema, sudden wgt gain
 Assess for rise in serum creatinine and
BUN values
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